| First Author | Splichalova I | Year | 2021 |
| Journal | Eur J Immunol | Volume | 51 |
| Issue | 9 | Pages | 2237-2250 |
| PubMed ID | 34107067 | Mgi Jnum | J:309562 |
| Mgi Id | MGI:6758615 | Doi | 10.1002/eji.202049142 |
| Citation | Splichalova I, et al. (2021) Deletion of TLR2(+) erythro-myeloid progenitors leads to embryonic lethality in mice. Eur J Immunol 51(9):2237-2250 |
| abstractText | Early embryonic hematopoiesis in mammals is defined by three successive waves of hematopoietic progenitors which exhibit a distinct hematopoietic potential and provide continuous support for the development of the embryo and adult organism. Although the functional importance of each of these waves has been analyzed, their spatio-temporal overlap and the lack of wave-specific markers hinders the accurate separation and assessment of their functional roles during early embryogenesis. We have recently shown that TLR2, in combination with c-kit, represents the earliest signature of emerging precursors of the second hematopoietic wave, erythro-myeloid precursors (EMPs). Since the onset of Tlr2 expression distinguishes EMPs from primitive progenitors which coexist in the yolk sac from E7.5, we generated a novel transgenic "knock in" mouse model, Tlr2(Dtr) , suitable for inducible targeted depletion of TLR2(+) EMPs. In this model, the red fluorescent protein and diphtheria toxin receptor sequences are linked via a P2A sequence and inserted into the Tlr2 locus before its stop codon. We show that a timely controlled deletion of TLR2(+) EMPs in Tlr2(Dtr) embryos results in a marked decrease in both erythroid as well as myeloid lineages and, consequently, in embryonic lethality peaking before E13.5. These findings validate the importance of EMPs in embryonic development. |
